Overview:
The severe acute respiratory syndrome-coronavirus
(SARS-CoV) is a single-stranded, positive-sense,
enveloped RNA virus that causes
severe acute
respiratory syndrome (Figure
1).
The virion consists of a spherical capsid 80 to
120 nm (namometres) in diameter, and can be
pleomorphic. It has a genome of
approximately 29740 nucleotide bases enclosed
within a helical nucleocapsid. The structural
proteins of SARS-CoV include: the surface spike
(S) glycoprotein, the membrane (M) protein, the
small envelope (E) glycoprotein, and the
nucleocapsid (N) protein (Wu et al.,
2004) (Figure 2). The spike protein appears on the surface
of the viral capsid or viral envelope, giving
the virus a crown-like (corona) appearance when
viewed under an electron microscope (Figure
1).
The M protein has a cytoplasmic tail and short
N-terminal ectodomain; there are only three M
proteins on the membrane. The E protein is
highly hydrophobic, while the S protein plays a
critical role in the attachment to target host
cells.

Symptoms & Diagnosis: The SARS-CoV causes acute
infections. Infected individuals may
experience common symptoms such as: chills,
muscle rigidity, malaise, headache,
fatigue, dry cough, muscle pain and varying
degrees of dyspnea. In addition, less common
symptoms include: sore throat, sputum
production, rhinorrhea, and
gastrointestinal complications. The most commonly
reported symptom amongst
all individuals infected with the
virus is a fever of 38°C or
higher. The diagnostic criteria used to
determining whether an individual is infected with
SARS is based the
aforementioned high fever. Also, since the
incubation period of the virus ranges
from two to ten days, direct or indirect contact
with previously infected individuals
pose as high risk for contracting the virus. An
individual who has recently
travelled to an area of high risk is
more susceptible to experiencing diagnostic
symptoms. The virus can affect
people of all age groups. Infection is rare in
adults; however, there is
insufficient empirical data to determine the
extent of infection on children and elderly
people. There is data that supports a higher
degree of susceptibility in
females than in males.

Pathogenicity:
SARS-CoV targets pneumocytes,
enterocytes, and endothelial cells in the host's airways by manipulating ACE-2
(Angiotensin-converting enzyme) receptors,
which are integral to the
rennin-angiotension pathway. The virus uses the
S protein as a ligand to bind to the receptor,
which allows the virus to fuse with the host cell membrane, resulting in immediate
infection. The S protein may
also mediate pH-dependent endocytosis as an
alternative entry mechanism.
The exact mechanism in which SARS-CoV causes
injury is still unknown;
however, a three-stage disease model was proposed,
illustrating that the virus acts in
three phases: viral replication, immune
hyperactivity, and pulmonary
destruction. The lung is a major site of viral
infection, where alveolar damage,
epithelial cell proliferation, and macrophage
concentration increase has been
observed. It has been proposed that much of the
inflicted pathogenicity is
attributed to increased proinflammatory cytokine
production as a result of the
increase in macrophage recruitment. Infected
individuals have been found to
have lymphopenia, hemophagocytosis (lung), and
white-pulp atrophy (spleen)
which were all characteristic of influenza
subtype H5N1. The infectious dose is
unknown; however, it is proposed that a single
viroid in the lungs may be
enough to cause infection.

Transmission:
The primary route of transmittance is
through respiratory droplets
spread via sneezing and coughing, where the
particles travel short distances to
land in proximity of mucous membranes of the eyes,
mouth, or nose. Likewise, contact of the
eyes, mouth, or nose by hands previously in
contact with infected surfaces or
objects are also a common spread of the
infection.

It has also been found that
the SARS-CoV is detectable in perspiration, and
thus can be spread by
individuals in contact with another individual
who is perspiring or has
perspired. This is why it is important to
disinfect all gym equipment before and after
use. Since there is no known vaccine,
control of the pathogen would be to
minimize and/or inhibit the routes of infection.
Wearing medical face masks,
minimizing contact with commonly touched
surfaces or objects, and wearing
latex gloves when in public can greatly reduce
the risk of infection; other
control measures, such as elimination of
hospital transmission via enhanced
infection-control methods have been utilized to
control pathogenic outbreaks. There have been developments of potential vaccines that target
and neutralize
the S protein to prevent attachment of the virus
to host cells (spike-specific
monoclonal and polyclonal antibodies) (Figure
3).

Figure 3.
Spike-specific monoclonal and polyclonal
antibodies preventing the uptake of the SARS-CoV
by binding to ACE-2 receptors and antagonizing
the viral-mediated response.